Cardiology Flashcards

Question

What is PCI with coronary angioplasty ?

Answer 1

PCI with coronary angioplasty is offered to all patients with proximal or extensive disease on CT coronary angiography. A catheter is inserted into the brachial or femoral artery which is fed up into the coronary arteries under X ray guidance. Contrast is used to see the areas of stenosis. This can be treated with balloon dilation followed by the insertion of a stent

Answer 2

The chest is opened along the sternum. A graft vein is taken from the pts leg (usually great saphenous vein) and sewing it onto the affected coronary artery to bypass the stenosis.

Answer 3

Right atrium Right ventricle Inferior aspect of left ventricle Posterior septal area

Answer 4

Left atrium Posterior aspect of left ventricle

Answer 5

Anterior aspect of left ventricle Anterior aspect of the septum

Answer 6

Perform an ECG

Answer 7

ST elevation in leads consistent with an area of ischaemia or New left BBB

Answer 8

T wave inversion in a specific region Pathological Q waves ST depression - This suggests a deep infarct and is a late sign

Answer 9

N+V Sweating and clamminess Feelings of impending doom Shortness of breath Palpitations Pain radiating to the jaw or arms

Answer 10

Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina.

Answer 11

Diabetic patients. They can experience a "silent MI"

Answer 12

Anterolateral I, aVL, V3-6

Answer 13

Anterior V1-4

Answer 14

Lateral I, aVL, V5-6

Answer 15

Inferior II, III, aVF

Answer 16

Proteins found in cardiac muscle

Answer 17

Serial troponins e.g. at baseline and 6 or 12 hours after the onset of symptoms

Answer 18

As troponin is released from ischaemic heart muscle

Answer 19

Raised troponin does not automatically mean ACS

Answer 20

Chronic renal failure Sepsis Myocarditis PE Aortic dissection

Answer 21

Chest Xray - to investigate for pulmonary oedema and other causes of chest pain Echocardiogram - after the event to assess the functional damage to the heart CT coronary angiogram - to assess for coronary artery disease

Answer 22

Primary PCI (if available within 2 hours of presentation) Thrombolysis (if PCI not available within 2 hours) -Immediate dual antiplatelet therapy (DAPT; aspirin plus Ticagrelor, Prasugrel, or Clopidogrel) and pain relief. Paramedics usually give the Aspirin and opiates. Oxygen should be avoided and nitrates are useless for MI. -Anticoagulation for 24-72hrs; Heparin, Fondapariux or similar -Both STEMI and NSTEMI should have angiography and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications -Secondary prevention; DAPT for a year then Aspirin alone, Statin, Betablocker for a year, ACE inhibitor, and treatment of any complication (heart failure, arrhythmia, etc). Cardiac rehabilitation; exercise, education, diet, smoking cessation

Answer 23

It involves injecting a fibrinolytic medication that rapidly dissolves clots. Examples = alteplase, streptokinase and tenecteplase

Answer 24

BATMA Beta blocker - unless contraindicated Aspirin - 300mg stat dose Ticagrelor - 180mg stat dose (clopidogrel 300mg is an alternative) Morphine - titrate to control pain Anticoagulant: LMWH at treatment dose Give oxygen only if oxygen saturations are dropping (i.e. <95%)

Answer 25

GRACE score

Answer 26

6 month risk of death or repeat MI after having an NSTEMI <5% = low risk 5-10% = medium risk >10% = high risk If the patient is medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

Answer 27

DREAD Death Rupture of the heart septum or papillary muscles oEdema (heart failure) Arrhythmia and aneurysms Dressler's syndrome

Answer 28

It usually occurs 2-3 wks following an MI. It is caused by a localised immune response and causes pericarditis .

Answer 29

Pleuritic chest pain, low grade fever and pericardial rub on auscultation Pericardial effusion and rarely a pericardial tamponade

Answer 30

ECG - global ST elevation and T wave inversion Echocardiogram - pericardial effusion Inflammatory markers - CRP, ESR

Answer 31

NSAIDS (aspirin, ibuprofen) In more severe cases - steroids (prednisolone) Pt may need pericardiocentesis to remove fluid from around the heart

Answer 32

6 A's Aspirin 75mg OD Another antiplatelet e.g. clopidogrel or ticagrelor for up to 12 months Atorvastatin 80mg OD ACEi (e.g. ramipril titrated as tolerated to 10mg OD) Atenolol (or other B blocker titrated as high as tolerated) Aldosterone antagonist for those with CHF (i.e. eplerenone titrated to 50mg OD) Dual antiplatelet therapy duration will vary following PCI procedures depending on the type of stent that was inserted

Answer 33

Stop smoking Reduce alcohol consumption Mediterranean diet Cardiac rehabilitation (a specific exercise regime for patients post MI) Optimise treatment of other medical conditions e.g. HTN, diabetes

Answer 34

When the left ventricle is unable to adequately move blood through the left side of the heart and out into the body.

Answer 35

Pulmonary oedema (when lung tissue and alveoli become full of interstitial fluid) There is a backlog of blood from the left ventricle that increases the amount of blood in the LA, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid into the surrounding tissues and are unable to reabsorb it. This interferes with normal gas exchange in the lungs causing shortness of breath, reduced oxygen saturation and the other S+S.

Answer 36

Iatrogenic (e.g. aggressive IV fluids in frail elderly pt with impaired LV function) Sepsis MI Arrhythmias

Answer 37

Rapid onset breathlessness. This is exacerbated by lying flat and improves on sitting up. Type 1 respiratory failure

Answer 38

SOB Looking and feeling unwell Cough with frothy white or pink sputum

Answer 39

Increased RR Decreased oxygen sats Tachycardia 3rd heart sound Bilateral basal crackles "sounding wet" on auscultation Hypotension in severe cases (cardiogenic shock)

Answer 40

Chest pain in ACS Fever in sepsis Palpitations with arrhythmias

Answer 41

Raised JVP Peripheral oedema in the ankles, legs and sacrum

Answer 42

History Clinical exam ECG - to look for ischaemia and arrhythmias ABG CXR Routine bloods for infection, kidney function, BNP and consider troponin if suspect MI Echocardiogram If the clinical presentation is acute LVF then initiate treatment before having the diagnosis confirmed by BNP or echo. Pts can deteriorate quickly.

Answer 43

A hormone that is released from the ventricles when the myocardium is stretched beyond normal range. A high BNP blood test result indicates that the heart is overloaded.

Answer 44

It causes the smooth muscle in blood vessels to relax which reduces systemic vascular resistance. It also acts on the kidneys as a diuretic. Both of these effects make it easier for the heart to pump blood around the body.

Answer 45

Tachycardia Sepsis PE Renal impairment COPD

Answer 46

It assesses the function of the LV and identifies any structural abnormalities in the heart. The mean measure of LV function is the ejection fraction. Above 50% is considered normal.

Answer 47

When the cardiothoracic ratio is more than 0.5 - when the diameter of the widest part of the heart is more than half the diamter of the widest part of the lung fields

Answer 48

Normally when stand erect the lower lobe veins contain a lot more blood than the upper lobes which remain relatively small. In LVF the backlog of blood causes the upper lobes to fill up and become engorged. This is visible as increased prominence and diameter of the upper lobe vessels on CXR.

Answer 49

Bilateral pleural effusions Fluid in interlobar fissures Fluid in the septal lines (Kerley lines)

Answer 50

Pour SOD Pour away (stop) their IV fluids Sit up - sit the patient upright as gravity takes fluid in the lungs to the bases leaving the upper lungs clear for better gas exchange Oxygen - if the pts sats are falling below 95% Diuretics - e.g. IV furosemide 40mg stat Also monitor fluid balance

Answer 51

IV opiates - opiates such as morphine act as vasodilators but are not routinely recommended Non-invasive ventilation - Would try CPAP first. Then if this doesn't work the pt may need full intubation and ventilation. Inotropes - For example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve HF however they need close titration and monitoring so by this point you would need to send the pt to a the local coronary unit, high dependency unit or ICU.

Answer 52

Basically just the chronic version of acute heart failure. Is either caused by impaired LV contraction (systolic heart failure) or impaired LV relaxation (diastolic heart failure).

Answer 53

-Breathlessness worsened by exertion -Cough. They may produce frothy white/ pink sputum. -Orthopnoea. This s the sensation of SOB when lying flat, relieves by sitting or standing. Ask them how many pillows they use at night. -Paroxysmal nocturnal dyspnoea -Peripheral oedema

Answer 54

A term used to describe the experience that pts have of suddenly waking at night with a severe attack of SOB

Answer 55

Clinical presentation BNP blood test specifically the N-terminal pro-B-type natriuretic peptide (NT-proBNP) Echocardiogram ECG

Answer 56

Ischaemic heart disease Valvular heart disease (commonly aortic stenosis) HTN Arrhythmias (commonly AF)

Answer 57

-Refer to specialist (NT-proBNP > 2000ng/litre warrans an urgent referral) -Careful discussion and explanation of the condition -Medical management -Surgical treatment in severe aortic stenosis or mitral regurgitation -HF specialist nurse input for advice and support Additional information: -Yearly flu and pneumococcal vaccine -Stop smoking -Optimise treatment of co morbidities -Exercise as tolerated

Answer 58

(ABAL) ACEi (e.g. ramipril titrated as tolerated up to 10mg OD) B blocker (e.g. bisoprolol titrated as tolerated up to 10mg OD) Aldosterone antagonist - when symptoms not controlled with A and B (spironolactone or epelerone) Loop diuretics (e.g. furosemide 40mg OD) Extra details on medical treatment: -An ARM can be used instead of ACEi if they are not tolerated e.g. candesartan - Avoid ACEi in patients with valvular heart disease until initiated by specialist -Pts should have their U&Es monitored closely whilst on diuretics, ACEi and aldosterone antagonists as all three medications can cause electrolyte disturbances.

Answer 59

Right sided HF caused by respiratory disease. Pulmonary HTN results in the right ventricle not being able to pump blood out of the ventricle and into the pulmonary arteries due to the increased pressure and resistance. This leads to back pressure of blood in the right atrium, vena cava and the systemic venous system.

Answer 60

COPD is the most common cause PE Interstitial lung disease Cystic fibrosis Primary pulmonary HTN Note: Lung diseases that cause hypoxia over a long period of time can lead to cor pulmonale as hypoxia causes an increase in resistance in the pulmonary circulation leading to an increase in the pressure etc etc.

Answer 61

Often pts with early cor pulmonale are asymptomatic. The main PC is SOB. Unfortunately SOB is also caused by the chronic lung diseases that cause CP. Pts may also present with peripheral oedema, increased breathlessness on exertion, syncope or chest pain.

Answer 62

Hypoxia Cyanosis Raised JVP Peripheral oedema Third heart sound Murmurs Hepatomegaly

Answer 63

Involves treating the symptoms and the underlying cause. Long term oxygen therapy is often used.

Answer 64

HTN that has developed on its own without a secondary cause. Accounts for 95% of HTN.

Answer 65

ROPE Renal disease - most common cause of secondary HTN. If the BP is very high or doesn't respond to treatment consider renal artery stenosis. Obesity Pregnancy induced HTN/ pre-eclampsia Endocrine - most endocrine conditions can cause HTN but primarily consider hyperaldosteronism (Conn's syndrome). A simple test for this is a renin:aldosterone ratio blood test.

Answer 66

Ischaemic heart disease Cerebrovascular accident i.e. stroke or haemorrhage Hypertensive retinopathy Hypertensive nephropathy Heart failure

Answer 67

Can be made based on several readings in the clinic, 24 hour ambulatory blood pressure or home readings. The latest thinking is that home readings taken by the patient at different times throughout the day are the gold standard. Stage 1 HTN, Clinic reading > 140/90, Home reading >135/85 Stage 2 HTN, Clinic reading > 160/100, Home reading >155/95

Answer 68

Investigate for possible causes and end organ damage. Advice on lifestyle including diet, reducing salt intake to under 6g per day, stopping smoking and taking regular exercise

Answer 69

Step 1: Aged less than 55 and non-black use an ACEi. Aged over 55 or black use CCB. Step 2: Non-black use A+C. If black then use ARB instead of ACEi. Step 3: ACEi + CCB + Thiazide like diuretic Step 4 : ACEi + CCB + Thiazide like diuretic + Diuretic For step 4 if the serum potassium is more than 4.5 mmol/L then the added diuretic is a higher dose thiazide diuretic e.g. indapamide. If the serum potassium is below 4.5 then the added diuretic is a potassium sparring diuretic e.g. spironolactone (this is helpful when thiazide diuretics are causing hypokalaemia). IMPORTANT: Monitor U&Es regularly when using ACEi + diuretic

Answer 70

< 80 years, systolic target < 140, diastolic target < 90 >80 years, systolic target < 150, diastolic target < 90 Note: These are likely to be lowered when the next set of guidelines are released. The last set for HTN was in 2011.

Answer 71

First line treatment = ACEi in everyone except: -Women with child bearing potential = CCB -Black pts: ACEi + CCB

Answer 72

Heard roughly 0.1 seconds after S2. Think of it as rapid ventricular filling causing the chordae tendineae to pull to their full length and twang like a guitar string. Can be normal in young healthy people (15-40) as the heart functions so well that the ventricles allow rapid filling. Can indicate HF in older patients as the ventricles and chordae are stiff and weak so they reach their limit much faster than normal. Picture tight hamstrings in an older pt sharply tightening as they start to bend over.

Answer 73

Always abnormal and rare to hear. It occurs just after atrial contraction and immediately before the systolic S1 and is caused by the atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle.

Answer 74

Bell = low pitched (church bell) Diaphragm = high pitched

Answer 75

Mitral - 5th ICS mid-clavicular line Tricuspid - 5th ICS left sternal border Pulmonary - 2nd ICS left sternal border Aortic - 2nd ICS right sternal border

Answer 76

3rd ICS left sternal border. Best area for listening to S1&S2.

Answer 77

-Patient on their left hand side (mitral stenosis) -Patient sat up, leaning forward and holding exhalation (aortic regurgitation)

Answer 78

SCRIPT Site - Where is the murmur the loudest? Character - soft/blowing/crescendo/decrescendo/crescendo-decrescendo Radiation Intensity - What grade is the murmur? Pitch Timing - Is it systolic or diastolic?

Answer 79

1. Difficult to hear 2. Quiet 3. Easy to hear 4. Easy to hear with palpable thrill 5. Can hear with stethoscope barely touching chest 6. Can hear with stethoscope off the chest

Answer 80

"This pt has a soft/harsh/blowing, Grade ..., systolic/ diastolic murmur, heard loudest in the aortic/ mitral/ tricuspid/ pulmonary area, that does not/ radiates to the carotids/ left axilla. It is high/ low pitched and has a crescendo/ decrescendo/ c+d shape. This is suggestive of a diagnosis of mitral stenosis / aortic stenosis"

Answer 81

Mitral stenosis causes left atrial hypertrophy Aortic stenosis causes left ventricular hypertrophy Mitral regurgitation causes left atrial dilation Aortic regurgitation causes left ventricular dilation (blood leaking back stretches the heart muscle resulting in dilation)

Answer 82

Rheumatic fever Infective endocarditis

Answer 83

-Mid-diastolic, low pitched "rumbling" murmur due to a low velocity of blood flow. -There will be a loud S1 due to the thick valves requiring a large systolic fore to shut, then shutting suddenly. -You can palpate a tapping apex beat, due to loud S1.

Answer 84

Malar flush - due to the back-pressure of blood in the pulmonary system causing a rise in CO2 and vasodilation AF - Due to the LA struggling to push blood through the stenotic mitral valve causing strain, electrical disruption and resulting fibrillation

Answer 85

-Idiopathic weakening of valve with age -Ischaemic heart disease -Infective endocarditis -Rheumatic fever -Connective tissue disorders such as Marfan syndrome or Ehlers Danlos syndrome

Answer 86

-Pan systolic, high pitched "whistling" murmur -The murmur radiates to the left axilla It results in CCF because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart. Therefore you may hear a 3rd heart sound.

Answer 87

-Age related idiopathic calcification -Rheumatic fever

Answer 88

- Ejection systolic, high pitched murmur - Crescendo-decrescendo character as blood flow is slowest at the start and end and fastest in the middle -Radiates to carotids - Slow rising pulse and narrow pulse pressure - Pts may complain of exertional syncope due to difficulty maintaining good flow to the brain

Answer 89

Idiopathic age related weakness Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

Answer 90

- Early-diastolic, soft murmur - Is also associated with a Corrigan's pulse (AKA collapsing pulse). A Corrigan's pulse is a rapidly appearing and disappearing pulse at the carotids as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve an into the ventricles. - Can cause a "Austin-Flint" murmur. This is heard at the apex and is an early diastolic "rumbling" murmur due to blood flowing back through the aortic vlave and over the mitral valve causing it to vibrate.

Answer 91

Heart failure due to a back pressure of blood waiting to get through the left side of the heart.

Answer 92

Midline sternotomy Lateral thoracotomy

Answer 93

Bioprosthetic - Around ten years Mechanic - Well over twenty years but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 to 3.5.

Answer 94

Starr Edwards valve - no longer being implanted, high risk of thrombus formation Tilting disc valve - single tilting disk St Jude valve - two tilting metals discs, least risk of thrombus formation

Answer 95

Thrombus formation Infective endocarditis (infection in prosthesis) Haemolysis causing anaemia (as blood gets churned in the valve)

Answer 96

A click replaces S1 for metallic mitral valve A click replaces S2 for metallic aortic valve

Answer 97

A treatment for severe aortic stenosis. Usually in pts that are high risk for an open valve replacement operation. It involves local or general anaesthetic, inserting a catheter into the femoral artery and feeding a wire under Xray guidance to the location of their aortic valve, then inflating a balloon to stretch the stenosed aortic valve and implanting a bioprosthetic valve in the location of the aortic valve. Open surgery is still the first line option for younger fitter pts.

Answer 98

Not typically as the valve is bioprosthetic.

Answer 99

Disorganised electrical activity overrides the normal organised activity from the SA node meaning the contraction of the atria is uncoordinated, rapid and irregular. This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles resulting in: -Irregularly irregular ventricular contractions -Tachycardia -HF due to poor filling of the ventricles during diastole -Risk of stroke

Answer 100

There is a tendency for blood to collect in the atria and form blood clots. These can become emboli and travel to the brain and block cerebral arteries causing an ischaemic stroke.

Answer 101

Patients are often asymptomatic and AF is incidentally picked when when attending for other reasons. Presenting symptoms can be: -Palpitations -SOB -Syncope (dizziness or fainting) -Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)

Answer 102

AF and ventricular ectopics Can be differentiated: -Using an ECG -Ventricular ectopics disappear when the heart rate gets over a certain threshold. Therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.

Answer 103

-Absent P waves -Narrow QRS complex tachycardia -Irregularly irregular ventricular rhythm

Answer 104

Pts with AF who also have moderate to severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the AF.

Answer 105

AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis.

Answer 106

mrs SMITH Sepsis Mitral valve pathology (stenosis or regurgitation) Ischaemic heart disease Thyrotoxicosis Hypertension

Answer 107

Rate or rhythm control Anticoagulation to prevent stroke

Answer 108

In AF atrial contractions are not coordinated so the ventricles have to fill up by suction and gravity. This is considerably less efficient. The higher the HR the less time is available for the ventricles to fill with blood, reducing the cardiac output. The aim is to get the HR below 100 to extend the time during diastole when the ventricles can fill with blood.

Answer 109

-Reversible causes for their AF -Their AF is of new onset (within the last 48 hours) -Their AF is causing heart failure -They remain symptomatic despite being effectively rate controlled

Answer 110

1. B blocker is the first line 2. CCB (e.g. diltiazem, not preferable in HF) 3. Digoxin (only in sedentary people. It needs monitoring and there is a risk of toxicity)

Answer 111

-There is a reversible cause for their AF -Their AF is of new onset (within the last 48hrs) -Their AF is causing HF -They remain symptomatic despite being effectively rate controlled

Answer 112

To return the pt to a normal sinus rhythm. This can be done through a single cardioversion event that puts the pt back into a normal sinus rhythm or long term medical rhythm control that sustains a normal rhythm.

Answer 113

-Immediate if the AF has been present for less than 48 hrs or they are severely haemodynamically unstable. -Delayed cardioversion if the AF has been present for more than 48 hrs and they are stable.

Answer 114

A minimum of 3 wks prior to cardioversion. Anticoagulation is essential because during the 48 hrs prior to cardioversion they may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a stroke. They should have RATE CONTROL whilst waiting for cardioversion.

Answer 115

Pharmacological or electrical

Answer 116

-Flecanide -Amiodarone (the drug of choice in pts with structural heart disease)

Answer 117

The aim is to rapidly shock the heart back into sinus rhythm. This involves sedation or a general anaesthetic and using a cardiac defibrillator machine to deliver controlled shocks in an attempt to restore sinus rhythm.

Answer 118

-B blockers are first line for rhythm control -Dronedarone is second line for maintaining normal rhythm where pts have had successful cardioverison -Amiodarone is useful in pts with HF or LV dysfunction.

Answer 119

When the AF comes and goes in episode, usually not lasting more than 48hrs. They should be anticoagulated on their CHADSVASc score like any other AF pt.

Answer 120

This is where pts take a pill to terminate their AF only when they feel symptoms of AF starting. To be appropriate for this approach they need to have infrequent episodes without any underlying structural heart disease.

Answer 121

Flecanide. Avoid in atrial flutter as it can cause 1:1 AV conduction and resulting in a significant tachycardia.

Answer 122

About 1-2%

Answer 123

Is a calculation of how the prothrombin time of the pt compares with the prothrombin time of normal healthy adult. For example an INR of 2 indicates that the pt has a prothrombin time twice that of a normal healthy adult.

Answer 124

Cytochrome P450 system

Answer 125

INR needs close monitoring and the warfarin dose needs adjusting accordingly as the INR will be affected by other drugs that influence the activity of the P450 system such as antibiotics.

Answer 126

-Many foods, particularly those that contain vitamin K such as leafy green vegetables -Those that affect P450 such as cranberry juice and alcohol -This means it is important to monitor INR more closely when the pt changes medications or their diet.

Answer 127

- 1 to 3 days -Vitamin K

Answer 128

The cost of monitoring warfarin is much higher than apixaban. Also NOACS will be coming off patient over the next few years.

Answer 129

-No monitoring is required -No major interaction problems -Equal or slightly better than warfarin at preventing strokes in AF -Equal or slightly less risk of bleeding than warfarin

Answer 130

CHA2DS2VASc score

Answer 131

C - Congestive heart failure H - Hypertension A2 - Age > 75 (Scores 2) D - Diabetes S2 - Stroke or TIA previously (Scores 2) V - Vascular disease A - Age 65 - 74 S - Sex (female) 1 : consider anticoagulation >1 : offer anticoagulation

Answer 132

HAS-BLED H - Hypertension A - Abnormal renal and liver function S - Stroke B - Bleeding L - Labile INRs (whilst on warfarin) E - Elderly D - Drugs or alcohol The easiest way to calculate the HAS-BLED score is with an online calculator that will provide a risk of bleeding based on their score.

Answer 133

Shockable: -Ventricular fibrillation -Ventricular tachycardia Non-shockable: -Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse) -Asystole (no significant electrical activity)

Answer 134

-Consider up to 3 synchronised shocks -Consider an amiodarone infusion

Answer 135

Narrow complex (QRS < 0.12s) -Atrial fibrillation - rate control with B blocker or diltiazem (CCB) -Atrial flutter control rate with a B blocker -Supraventricular tachycardias - treat with vagal manoeuvres and adenosine Broad complex (QRS > 0.12s) -Ventricular tachycardia or unclear - amiodarone infusion -If known SVT with bundle branch block- treat as normal SVT -If irregular may be variation of AF - seek expert help

Answer 136

It is caused by a "re-entrant rhythm" in either atrium. This is where the electrical signal circulates in a self perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm. The signal makes its way into the ventricles every second lap due to the long refractory period of the AV node, causing 150 bpm ventricular contraction. It gives the "sawtooth appearance" on the ECG with P wave after P wave.

Answer 137

-HTN -Ischaemic heart disease -Cardiomyopathy -Thyrotoxicosis

Answer 138

Treatment is similar to AF: -Rate/rhythm control with B blockers or cardioversion -Treat the reversible underlying condition -Radiofrequency ablation of the re-entrant rhythm -Anticoagulation based on CHA2DS2VASc score

Answer 139

They are caused by the electrical signal re-entering the atria from the ventricles. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in a fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

Answer 140

Describes a situation where SVT reoccurs and remits in the same pt over time.

Answer 141

-"AV nodal re-entrant tachycardia" is when the re-entry point is back through the AV node -"AV re-entrant tachycardia" is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome) -"Atrial tachycardia" is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. The ectopic electrical activity causes an atrial rate of > 100bpm.

Answer 142

When managing SVT take a stepwise approach trying each step to see whether it works before moving on. Make sure they are on continuous ECG monitorig. -Valsalva manoeuvre - ask the pt to blow hard against resistance, for example into a plastic syringe. -Carotid sinus massage - massage the carotid on one side gently with two fingers -Adenosine -An alternative to adenosine is verapamil -Direct current cardioversion may be required if the treatment above fails

Answer 143

It works by slowing cardiac conduction primarily through the AV node. It interrupts the AV node / accessory pathway during SVT and "resets" it back to sinus rhythm.

Answer 144

It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway .

Answer 145

It will often cause a brief period of asystole or bradycardia however it is quickly metabolised and sinus rhythm should return.

Answer 146

-Avoid if patient has asthma, COPD, heart failure, heart block or severe hypotension -Warn the pt about the scary feeling of dying or impending doom when injected -Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa) -Initially 6mg, then 12mg and further 12mg if no improvement between doses.

Answer 147

Options are: -Medication (B blockers, CCB, amiodarone) -Radiofrequency ablation

Answer 148

Caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the AV node. The extra pathway that is present in WPW syndrome is often called the Bundle of Kent.

Answer 149

Radiofrequency ablation of the accessory pathway

Answer 150

-Short PR interval (<0.12 seconds) -Wide QRS complex (>0.12 seconds) -"Delta wave" (a slurred upstroke on the QRS complex).

Answer 151

If a pt has a combination of AF or atrial flutter and WPW there is a risk that the chaotic electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway.

Answer 152

Catheter ablation is performed in an electrophysiology laboratory, often called a "cath lab". It involves local or general anaesthetic, inserting a catheter into the femoral veins and feeding a wire through the venous system under Xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point to try and find the location of any abnormal electrical pathways. The operator may try and induce the arrhythmia to make the abnormal pathway easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity

Answer 153

-Atrial fibrillation -Atrial flutter -Supraventricular tachycardias -WPW syndrome

Answer 154

It is a type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as "twisting of the tips", describing the ECG characteristics. It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes get progressively smaller than larger then smaller and so on. It occurs in pts with a prolonged QT interval which is an ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction. Waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of the heart myocytes. These abnormal spontaneous depolarisations prior to repolarisation are known as "afterdepolarisations". These afterdepolarisations spread throughout the ventricles leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called torsades de pointes. When a pt develops torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest

Answer 155

-Long QT syndrome (inherited) -Medications such as antipsychotics, citalopram, flecanide , sotalol, amiodarone and macrolide antibiotics -Electrolyte disturbances such as hypokalaemia, hypomagnesaemia and hypocalcaemia

Answer 156

-Correct the cause (electrolyte disturbances or medications) -Magnesium infusion (even if they have a normal magnesium) -Defibrillation if VT occurs

Answer 157

-Avoid medications that prolong the QT interval -Correct electroyte disturbances -B blockers (not sotalol) -Pacemaker or implantable defibrillator

Answer 158

Premature ventricular beats caused by random electrical discharges from outside the atria. Pts often present complaining of random brief palpitations ("an abnormal beat").

Answer 159

They are relatively common at all ages and in healthy pts however they are more common in pts with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure)

Answer 160

On an ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG

Answer 161

This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.

Answer 162

-Check bloods for anaemia, electrolyte disturbances and thyroid abnormalities -Reassurance and no treatment in otherwise healthy people -Seek expert advice in pts with background heart conditions or other concerning features or findings such as chest pain, syncope, murmur or family history of sudden death

Answer 163

It's when there is delayed atrioventricular conduction through the AV node. Despite this every atrial impulse leads to a ventricular contraction, meaning every p waves results in a QRS complex. On an ECG this presents as a PR interval greater than 0.2 seconds (5 small or 1 big square)

Answer 164

It's when some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes. There are three patterns of second degree heart block: -Wenckebach's phenomenon (Mobitz Type 1) -Mobitz Type 2 -2:1 Block

Answer 165

This is where the atrial impulses become gradually weaker until they don't pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats. On an ECG this will appear as an increasing PR interval until the P wave no longer conducts to the ventricles. This culminates in an absent QRS complex after a p wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle then repeats itself.

Answer 166

This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of p waves to QRS complexes, for example 3 p waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal. There is a risk of asystole with Mobitz Type 2.

Answer 167

This is where there 2 p waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. This can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.

Answer 168

This is referred to as a complete heart block. There is no observable relationship between p waves and QRS complexes. There is a significant risk of aystole.

Answer 169

Fist line: -Atropine 500mcg IV No improvement: -Atropine 500mcg IV (repeated up to 6 doses for a total to 3mg) -Other inotropes (such as noradrenalin) -Transcutaneous cardiac pacing (using a defibrillator)

Answer 170

-Temporary transvenous cardiac pacing - using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly -Permanent implantable pacemaker - when available

Answer 171

It is an antimuscarinic medication that works by inhibiting the parasympathetic nervous system. -Pupil dilation -Urinary retention -Dry eyes -Constipation

Answer 172

They deliver controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve the heart function. They consist of a pulse generator (the little pacemaker box) and pacing leads that carry electrical impulses to the relevant part of the heart. The box is implanted under the skin (most commonly the left anterior chest wall or axilla) and the wires are implanted into the relevant chambers of the heart. Modern pacemakers have a computer that monitors the natural electrical activity and tailors its function to that. Basically if it is already working perfectly, no intervention is provided by the pacemaker. The batteries last around 5 years.

Answer 173

In short no. They may be a contraindication for MRI (due to powerful magnets) and electrical interventions such as TENS machines and diathermy in surgery. Many modern pacemakers are MRI compatible.

Answer 174

Pacemakers need to be removed prior to cremation. They can cause significant damage if burned.

Answer 175

-Symptomatic bradycardias -Mobitz type 2 AV block -Third degree heart block -Severe heart failure (biventricular pacemakers) -Hypertrophic obstructive cardiomyopathy (ICDs)

Answer 176

They have leads in a single chamber either the RA or the RV. They are placed in the RA if the AV conduction in the pt is normal and the issue is with the SA node. This way they stimulate depolarisation in the RA and this electrical activity then passes to the LA and through the AV node to the ventricles in the normal way. They are placed in the right ventricle if the AV conduction in the pt is abnormal and they stimulate the ventricles directly.

Answer 177

They have leads in both the RA and RV. This allows the pacemaker to synchronise the contractions of both the atria and ventricles

Answer 178

They have leads in the RA, RV and LV. These are usually in pts with HF. The objective is to synchronise the contractions in these chambers to try to optimise heart function. They are also called cardiac resynchronisation therapy (CRT) pacemakers.

Answer 179

They continually monitor the heart and apply a defibrillator shock to cardiovert the pt back into sinus rhythm if they identify a shockable arrhythmia.

Answer 180

The pacemaker intervention can be seen as a sharp vertical line on all leads of the ECG trace. A line before the p wave indicates a lead in the atria. A line before each QRS complex indicates a lead in the ventricles. Therefore: -A line before either the P or QRS but not the other indicates a single-chamber pacemaker -A line before both the P and QRS indicates a dual-chamber pacemaker.